Sleep-deprived cognitive impairment in aging mice is alleviated by rapamycin

I have found this very true in my case also - I am much more resilient when faced with sleep deprivation, and much more energy throughout the day until late at night.

Seems like something the military (Ukraine Military…) would benefit from…

Sleep deprivation-induced cognitive impairment is a major health concern and an age-related risk factor for dementia. There is an urgent need to develop ways of preventing the adverse neurological effects of sleep deprivation, but current preclinical animal models of short-term sleep deprivation are not well described.

Methods: C57BL6 mice of varying ages were sleep deprived for 4 hours a day for 4 days, and then tested with a Box maze navigation task.

Results: Sleep deprived mice at young, middle and older ages showed learning impairment that varied by strain and gender. In general, females of both strains were more sensitive to sleep deprivation than males. To determine whether sleep deprivation-induced learning impairment would respond to therapeutic intervention, an independent cohort of mice was treated with rapamycin daily during the 4 days of sleep deprivation. Mice that were sleep deprived and treated with rapamycin showed significant improvement in learning time suggesting that the cognitive impairment might be associated in part with molecular and cellular mechanisms targeted by rapamycin.

Conclusions: The observations from this study suggest that aging mice would be productive models to study pathobiology and therapeutic intervention of cognitive impairment triggered by age-related sleeping disorders in people.

Full Paper:

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Rapamycin, the magical drug. Who knows what benefit they will uncover next?

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I believe creatine does something similar:

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Funny to stumble on this post after I had 3 nights with 3-5 hours of sleep. I didn’t function at all and was sitting behind my laptop frustrated to not be able to think well, so Rapa didn’t seem to alleviate this for me unfortunately :melting_face:

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I am quite surprised that more forum members have not reported improvement in sleep time and quality.
After taking rapamycin for several months my sleep time and quality greatly improved.
Now I have no problem getting 7-8 hrs of good sleep. Rapamycin has reduced my large sleep stack to melatonin only.

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I started on working to improve my health because I had serious insomnia. A lot of that came from being a really heavy drinker of alcohol. I have, therefore, experimented with all sorts of approaches on sleep.

One thing I find to be the case is that even if I don’t sleep that many hours a largeish amount of melatonin taken during the night (never before I go to sleep) assists in improving cognitive function. I only take melatonin to extend sleep.

When I say largish I mean something like 30-40mg minimum. My record melatonin consumption in any one night is just over 900mg, but I take some suppositories of 400 or 200mg partially to increase mitochondrial melatonin as well as various 10mg pills.

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Yes - I had the same experience.

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It would be interesting to see if rapamycin reverses the lifspan shortening effects of shift work. I know lots of ER doctors and residents that could benefit…

Acute sleep deprivation exacerbates systemic inflammation and psychiatry disorders through gut microbiota dysbiosis and disruption of circadian rhythms

Acute sleep deprivation (ASD) is often observed in shift workers and characterized by drowsiness and unrelenting exhaustion. The physiological and psychological effects of ASD include anxiety, depression, cognitive impairment, systemic inflammation, stress responses, and disruptions of gut microbiota. However, the mechanisms involved in the ASD-associated circadian dysregulations with regard to gut dysbiosis, systemic inflammation, physiological modulation, and psychiatry disorders remain unclear. The aim of this study was to investigate whether central nervous system disorders induced by ASD are related to inflammation, barrier dysfunction, and circadian dysregulation. We also assessed impacts on microbiota succession. Male C57BL/6 mice were randomly allocated to the control and sleep deprivation (SD) groups. Mice in the SD group were subjected to 72 h of paradoxical SD using the modified multiple-platform method for ASD induction (72 h rapid eye movement-SD). The effects of ASD on dietary consumption, behaviors, cytokines, microbiota, and functional genes were determined. The SD group demonstrated significantly higher appetite and anxiety-like behaviors but significantly lower body weight than the control group

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